QuicKey Human MAU(Microalbuminuria) ELISA Kit

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This ELISA kit uses the Sandwich-ELISA principle. The micro ELISA plate provided in this kit has been pre-coated with an antibody specific to Human MAU. Samples (or Standards) and biotinylated detection antibody specific for Human MAU are added to the micro ELISA plate wells. Human MAU would combine with the specific antibody. Then Avidin-Horseradish Peroxidase (HRP) conjugate are added successively to each micro plate well and incubated. Free components are washed away. The substrate solution is added to each well. Only those wells that contain Human MAU, biotinylated detection antibody and Avidin-HRP conjugate will appear blue in color. The enzyme-substrate reaction is terminated by the addition of stop solution and the color turns yellow. The optical density (OD) is measured spectrophotometrically at a wavelength of 450 ± 2 nm. The OD value is proportional to the concentration of Human MAU. You can calculate the concentration of Human MAU in the samples by comparing the OD of the samples to the standard curve.

An unopened kit can be stored at 2-8℃ for six months. After test, the unused wells and reagents should be stored according to the table below.

Intra-assay Precision (Precision within an assay): 3 samples with low, mid range and high level Human MAU were tested 20 times on one plate, respectively.
Inter-assay Precision (Precision between assays): 3 samples with low, mid range and high level Human MAU were tested on 3 different plates, 20 replicates in each plate.

The recovery of Human MAU spiked at three different levels in samples throughout the range of the assay was evaluated in various matrices.

Microalbuminuria is a subtle increase in the urinary excretion of the protein albumin that cannot be detected by a conventional assay. In diabetes, microalbuminuria is an early sign of diabetic kidney disease. Specifically, the excretion of greater than 30 mg and less than 300 mg a day of albumin in the urine. The normal urinary albumin is less than 30 mg per 24 hours and 300 mg or more of urinary albumin per day is considered gross albuminuria. The phenomenon of albuminuria has been recognized for more than 200 years, and its association with kidney disease dates to the epochal insights of Richard Bright in 1827[1]. Microalbuminuria is caused by glomerular capillary injury and so may be a marker for diffuse endothelial dysfunction. According to Steno hypothesis, albuminuria might reflect a general vascular dysfunction and leakage of albumin and other plasma macromolecules such as low density lipoproteins into the vessel wall that may lead to inflammatory responses and in turn start the atherosclerotic process [2].

1. Glassock R J. Prevention of Microalbuminuria in Type 2 Diabetes: Millimeters or Milligrams? [J]. Journal of the American Society of Nephrology Jasn, 2006, 17(12):3276.

2. Deckert T, Feldtrasmussen B, Borchjohnsen K, et al. Albuminuria reflects widespread vascular damage [J]. Diabetologia, 1989, 32(4):219.